The Relationship between Plasma Pentraxin 3 and Serum Amyloid P Levels and Disease Activity in Ankylosing Spondylitis.

Background: In clinical practice, it is hard to judge the level of disease activity in some patients with ankylosing spondylitis (AS) who have low traditional acute phase reactant values such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) but have considerable pain and inflammation. The aim of this study is to investigate plasma pentraxin 3 (PTX3) and serum amyloid P (SAP) levels in patients with AS who had normal ESR and CRP but high disease activity. Methods: 100 AS patients and 100 gender- and age-matched controls were included. Epidemiological, clinical, and treatment data and plasma levels of CRP, ESR, PTX3, and SAP were evaluated. The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Ankylosing Spondylitis Disease Activity Score (ASDAS)-CRP were used for evaluating disease activity. Plasma levels of PTX3 and SAP were compared between AS patients and controls and also among AS patients with active and inactive disease. Results: AS patients had significantly higher plasma levels of PTX3 and SAP than controls. There were not any significant correlations between PTX3 and SAP with BASDAI, ASDAS-CRP, and ESR. There was a positive correlation between PTX3 and CRP. No significant difference in plasma levels of PTX3 and SAP was observed between patients with active disease and inactive disease, both with normal ESR and CRP levels. Disease duration and treatment did not influence plasma PTX3 levels. Conclusions: In patients with AS, plasma levels of PTX3 and SAP were found to be elevated when compared to healthy controls. No association was observed between these biomarkers and disease activity.

Anti-tumor necrosis factor alpha treatment does not influence serum levels of the markers associated with radiographic progression in ankylosing spondylitis.

Objectives: The study aimed to determine the levels of change of the markers related to radiographic progression, such as Dickkopf-1 (DKK-1), sclerostin (SOST), bone morphogenetic protein (BMP)-2 and -4, and interleukin (IL)-17 and -23, in ankylosing spondyloarthritis (AS) during anti-tumor necrosis factor alpha (TNF-α) treatment. Patients and methods: Fifty-three anti-TNF-α naïve AS patients (34 males, 19 females; median: 38 years; range, 20 to 52 years) refractory to conventional treatments meeting the modified New York criteria or Assessment of SpondyloArthritis International Society classification criteria were enrolled to this cross-sectional, controlled study between October 2015 and January 2017. Fifty healthy volunteers (35 males, 15 females; median: 36 years; range, 18 to 55 years) with similar age and sex characteristics were recruited. Serum DKK-1, BMP-2, BMP-4, SOST, IL-17, and IL-23 levels were measured in both groups. The serum levels of the markers were measured again after about two years (mean follow-up duration of 21.7±6.4 months) in AS patients who started anti-TNF-α treatment. Demographic, clinical characteristics, and laboratory parameters were recorded. The disease activity at the time of inclusion was assessed through the Bath Ankylosing Spondylitis Disease Activity Index. Results: Serum DKK-1, SOST, IL-17, and IL-23 levels in the AS group before anti-TNF-a treatment were significantly higher compared to the control group (p<0.01 for DKK-1, p<0.001 for others). There was no difference regarding serum BMP-4 levels, whereas BMP-2 levels were significantly higher in the control group (p<0.01). Forty (75.47%) AS patients had serum marker levels measured after anti-TNF-α treatment. No significant change was observed in the serum levels of these 40 patients measured 21.7±6.4 months after the initiation of anti-TNF-α treatment (p>0.05 for all). Conclusion: In AS patients, there was no change in DKK-1/SOST, BMP, and IL-17/23 cascade with anti-TNF-α treatment. This finding may suggest that these pathways act independently of each other, and their local effects are not influenced by systemic inflammation.